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关于此项目
经验公式（希尔记法）:
C25H38O5
化学文摘社编号:
分子量:
418.57
NACRES:
NA.24
PubChem Substance ID:
UNSPSC Code:
41116107
MDL number:
InChI
1S/C25H38O5/c1-6-25(4,5)24(28)30-21-12-15(2)11-17-8-7-16(3)20(23(17)21)10-9-19-13-18(26)14-22(27)29-19/h7-8,11,15-16,18-21,23,26H,6,9-10,12-14H2,1-5H3/t15-,16-,18+,19+,20-,21-,23-/m0/s1
SMILES string
[H][C@]12[C@H](C[C@@H](C)C=C1C=C[C@H](C)[C@@H]2CC[C@@H]3C[C@@H](O)CC(=O)O3)OC(=O)C(C)(C)CC
InChI key
RYMZZMVNJRMUDD-HGQWONQESA-N
grade
pharmaceutical primary standard
API family
simvastatin
manufacturer/tradename
USP
technique(s)
HPLC: suitable, gas chromatography (GC): suitable
mp
127-132 °C (lit.)
application(s)
pharmaceutical (small molecule)
format
neat
Gene Information
human ... HMGCR(3156)
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General description
This product is provided as delivered and specified by the issuing Pharmacopoeia. All information provided in support of this product, including SDS and any product information leaflets have been developed and issued under the Authority of the issuing Pharmacopoeia.For further information and support please go to the website of the issuing Pharmacopoeia.
Application
Simvastatin USP reference standard, intended for use in specified quality tests and assays as specified in the USP compendia. Also, for use with USP monographs such as:
- Simvastatin Tablets
Biochem/physiol Actions
辛伐他汀是HMG-CoA还原酶和降胆固醇药物的特异性抑制剂。
辛伐他汀是HMG-CoA还原酶的特异性抑制剂，HMG-CoA还原酶是催化HMG-CoA转化为甲羟戊酸的酶，其是胆固醇生物合成的早期步骤。由于它可以降低低密度脂蛋白和甘油三酯的水平，并提高高密度脂蛋白水平，因而可用于治疗高胆固醇血症。辛伐他汀是一种内酯，其在体内 易于水解成相应的β-羟基酸，并可以在使用前用溶于EtOH中的NaOH进行活化。它是洛伐他汀的合成类似物（货M2147）。
Analysis Note
These products are for test and assay use only. They are not meant for administration to humans or animals and cannot be used to diagnose, treat, or cure diseases of any kind.
Other Notes
Sales restrictions may apply.
signalword
Warning
hcodes
Hazard Classifications
Repr. 2
存储类别
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
Joost Besseling et al.
JAMA, 313(10), 1029-1036 (2015-03-11)
Familial hypercholesterolemia is characterized by impaired uptake of cholesterol in peripheral tissues, including the liver and the pancreas. In contrast, statins increase the cellular cholesterol uptake and are associated with increased risk for type 2 diabetes mellitus. We hypothesize that
Peter J Kirkpatrick et al.
The Lancet. Neurology, 13(7), 666-675 (2014-05-20)
The benefit of statins in patients with acute aneurysmal subarachnoid haemorrhage is unclear. We aimed to determine whether simvastatin 40 mg could improve the long-term outcome in patients with this disorder. In this international, multicentre, randomised, double-blind trial, we enrolled
Anders M Greve et al.
Stroke, 45(7), 1939-1946 (2014-06-07)
There are limited data on risk stratification of stroke in aortic stenosis. This study examined predictors of stroke in aortic stenosis, the prognostic implications of stroke, and how aortic valve replacement (AVR) with or without concomitant coronary artery bypass grafting
Mark Screen et al.
The American journal of pathology, 184(8), 2322-2332 (2014-06-08)
Myotonic dystrophy type 2 (DM2) is a multisystemic disorder caused by a (CCTG)n repeat expansion in intron 1 of CNBP. Transcription of the repeats causes a toxic RNA gain of function involving their accumulation in ribonuclear foci. This leads to
A Marot et al.
Acta clinica Belgica, 66(2), 134-136 (2011-06-03)
Myopathy, including rhabdomyolysis, is a well-known, albeit rare complication of statin therapy. Predisposing factors include comorbidities and the concomitant use of cytochrome P-450 (CYP) 3A4 inhibitors. We report a case of severe simvastatin-induced rhabdomyolysis triggered by the addition of amiodarone
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